Molecular mechanisms of maize seedling response to La2O3 NP exposure: water uptake, aquaporin gene expression and signal transduction

2017 ◽  
Vol 4 (4) ◽  
pp. 843-855 ◽  
Author(s):  
Le Yue ◽  
Chuanxin Ma ◽  
Xinhua Zhan ◽  
Jason C. White ◽  
Baoshan Xing

We investigated the relative expressions of aquaporin genes and the levels of abscisic acid in maize upon exposure to La2O3 NPs.

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Chenxu Ye ◽  
Humaira Rasheed ◽  
Yuehua Ran ◽  
Xiaojuan Yang ◽  
Lianxi Xing ◽  
...  

Abstract Background The reproductive plasticity of termite workers provides colonies with tremendous flexibility to respond to environmental changes, which is the basis for evolutionary and ecological success. Although it is known that all colony members share the same genetic background and that differences in castes are caused by differences in gene expression, the pattern of the specific expression of genes involved in the differentiation of workers into reproductives remains unclear. In this study, the isolated workers of Reticulitermes labralis developed into reproductives, and then comparative transcriptomes were used for the first time to reveal the molecular mechanisms underlying the reproductive plasticity of workers. Results We identified 38,070 differentially expressed genes and found a pattern of gene expression involved in the differentiation of the workers into reproductives. 12, 543 genes were specifically upregulated in the isolated workers. Twenty-five signal transduction pathways classified into environmental information processing were related to the differentiation of workers into reproductives. Ras functions as a signalling switch regulates the reproductive plasticity of workers. The catalase gene which is related to longevity was up-regulated in reproductives. Conclusion We demonstrate that workers leaving the natal colony can induce the expression of stage-specific genes in the workers, which leads to the differentiation of workers into reproductives and suggests that the signal transduction along the Ras-MAPK pathway crucially controls the reproductive plasticity of the workers. This study also provides an important model for revealing the molecular mechanism of longevity changes.


2001 ◽  
Vol 276 (50) ◽  
pp. 47136-47142 ◽  
Author(s):  
Theresa D. Joseph ◽  
Dwight C. Look

Adenoviral evolution has generated strategies to resist host cell antiviral systems, but molecular mechanisms for evasion of interferon (IFN) effects by adenoviruses during late-phase infection are poorly defined. In this study, we examined adenovirus type 5 (AdV) effects on IFN-γ-dependent gene expression and Janus family kinase-signal transducer and activator of transcription signaling components in human tracheobronchial epithelial cells. We found that AdV infection specifically inhibited IFN-γ-dependent gene expression in airway epithelial cells without evidence of epithelial cell injury or generation of a soluble extracellular inhibitor. Furthermore, infection with AdV for 18–24 h blocked phosphorylation/activation of the Stat1 transcription factor that regulates IFN-γ-dependent genes. Although AdV also inhibited IFN-α-dependent phosphorylation of Stat1 and Stat2, interleukin-4-dependent phosphorylation of the related transcription factor Stat6 was not affected, indicating that the virus selectively affected specific signaling pathways. Our results indicate that AdV inhibition of the IFN-γ signal transduction cascade occurs through loss of ligand-induced receptor complex assembly and consequent component phosphorylation and suggest that lack of complex assembly is due to decreased expression of the IFN-γR2 chain of the IFN-γ receptor. IFN-γR2 is required at an early step in Janus family kinase-signal transducer and activator of transcription pathway activation and is expressed at low levels in airway epithelial cells, supporting the concept that adenoviral down-regulation of the level of this IFN-γ receptor component allows for persistent modulation of IFN-γ-dependent gene expression.


2019 ◽  
Author(s):  
Chenxu Ye ◽  
Humaira Rasheed ◽  
Yuehua Ran ◽  
Xiaojuan Yang ◽  
Lianxi Xing ◽  
...  

Abstract Background: The reproductive plasticity of termite workers provides colonies with tremendous flexibility to respond to environmental changes, which is the basis for evolutionary and ecological success. Although it is known that all colony members share the same genetic background and that differences in castes are caused by differences in gene expression, the pattern of the specific expression of genes involved in the differentiation of workers into reproductives remains unclear. In this study, the transition of the female workers into neotenic reproductives (NRs) was induced by a groups of isolated workers (IWs) of Reticulitermes labralis, and then comparative transcriptomes were used for the first time to reveal the molecular mechanisms underlying the reproductive plasticity of workers. Results: We identified 38,070 differentially expressed genes and found profile 5 to be the pattern of gene expression involved in the differentiation of the workers into reproductives. 12,543 genes were specifically upregulated in the IWs. Twenty-five signal transduction pathways classified into environmental information processing were related to the differentiation of workers into NRs. Ras functions as a signalling switch regulated the reproductive plasticity of workers.The catalase gene which is related to longevity was up-regulated in NRs. Conclusion: We demonstrate that workers leaving the natal colony can induce the expression of stage-specific genes in the workers, which leads to the differentiation of workers into queens and suggests that the signal transduction along the Ras-MAPK pathway crucially controls the reproductive plasticity of the workers. This study also provides an important model for revealing the molecular mechanism of longevity changes.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4311-4311
Author(s):  
Qingping Cui ◽  
Haesook Kim ◽  
Peter H. Wiernik ◽  
Martin S. Tallman ◽  
Robert E. Gallagher

Abstract This study was based on the hypothesis that a global comparison of gene expression levels between APL cells before treatment and at relapse might provide crucial information about molecular mechanisms involved in the selection of relapse clones. Matched samples were derived from 7 patients treated on protocol E2491 (randomization of newly diagnosed patients to either C alone or ATRA for induction and then to maintenance ATRA or observation after consolidation), 4 on A arms and 3 on the C arm. Comparable levels of promyeloblasts were present in the low-density mononuclear cell fraction derived from bone marrow (BM) or peripheral blood (PB) with 1 exception (Patient 4). RNA was prepared by a guanidinium-cesium chloride gradient procedure, and gene expression analysis utilized the Affymetrix Human Genome U-133 Plus 2.0 chip. For unsupervised hierarchical cluster analysis, the normalized data were filtered by the following criteria: coefficient of variation across samples (standard deviation/mean) 〉0.7 and expression level ≥100 in at least 50% of samples. Although there was considerable heterogeneity, 1415 filtered genes clustered into three groups (UCG; see table): #1 with 6 pretreatment patients, #2 with 3 relapse patients (2 C and 1 A), and #3 with 1 pretreatment and 4 relapse patients (1 C and 3 A). Derivation of RNA from PB cells may have contributed to UCG #2 clustering. By supervised analysis, using the criteria of a mean difference of ≥100 between the pretreatment and relapse values and a p-value <.01 by paired t-tests, 443 genes were selected with a median false discovery rate of 13%. To further select a robust and consistent set of genes, an ad-hoc ‘leave-one paired sample-out’ analysis was performed. 139 genes were selected across all 7 subsets and, for 116 genes, the difference between pretreatment and relapse values was ≥1.5-fold--40 upregulated (U) and 76 downregulated (D). The relapse changes in expression of named genes included those affecting signal transduction via ras-related genes (RASA1, D; RASSF1, U; RAB1B&5C, U; ARF6, U; RGS10, U) and protein kinase A (AKAP11, D; PRKAR1A, D), apoptosis (MAP3K5/ASK1, D; CFLAR/FLIP, D; FAF1, U; UBE2D2, U), chromatin (SMARCA2, D; SMARCB1, U; HNRPH3, D), cell division (ANAPC4, D; CDC2L6, D; CENPJ, D), interferon activity (IRF7, U), and microRNA synthesis (DICER1, D). Gene expression changes (>2.5-fold) in the 443 gene set included: HGF, 3.6xD; APAF1, 3.4xD; IRF1, 2.6xU; FOSL1, 2.7xU; TGFB1, 2.9xU; RELB, 3.7xU; MAFF, 4.3xU. Although highly diverse, these findings point to potentially drug-targetable alterations of AP-1 and NFΚB transcriptional control in association with alterations in ras- and PKA-regulated signal transduction pathways and possibly to microRNA synthesis as common molecular processes in APL cells related to disease progression and relapse.


2004 ◽  
Vol 286 (6) ◽  
pp. G1000-G1008 ◽  
Author(s):  
M. Mühlbauer ◽  
B. Allard ◽  
A. K. Bosserhoff ◽  
S. Kiessling ◽  
H. Herfarth ◽  
...  

Several effects of bile acids (BAs) on colonic epithelial cells (CECs) have been described, including induction of proliferation and apoptosis. Some of these effects are mediated through activation of the NF-κB transcriptional system. In this study, we investigated the molecular mechanisms underlying the BA-induced gene expression in CECs. The human CEC line HT-29 and primary human CECs were treated with dilutions of salts of deoxycholic acid (DCA) and taurodeoxycholic acid (TDCA). NF-κB binding activity was analyzed with EMSA, RelA translocation with immunofluorescence, and IκBα- and RelA-phosphorylation with Western blot analysis. IL-8 mRNA and protein expression were assessed by quantitative PCR and ELISA. Functional impact of NF-κB activation was determined by blocking the proteasome activity with MG132 or by preventing IKK activity with a dominant-negative IKKβ delivered by adenoviral dominant-negative (dn) IKKβ (Ad5dnIKKβ). DCA and TDCA induced IL-8 expression in a dose- and time-dependent manner. It is interesting that DCA but not TDCA induced IκBα-phophorylation, RelA translocation, and NF-κB binding activity. Accordingly, the proteasome inhibitor MG132 blocked DCA- but not TDCA-induced IL-8 gene expression. In contrast, TDCA-induced IL-8 gene expression correlated with enhanced RelA phosphorylation, which was blocked by Ad5dnIKKβ. Our data suggest that DCA-induced signal transduction mainly utilized the IκB degradation and RelA nuclear translocation pathway, whereas TDCA primarily induced IL-8 gene expression through RelA phosphorylation. These differences may have implications for the understanding of the pathophysiology of inflammation and carcinogenesis in the gut.


2019 ◽  
Author(s):  
Chenxu Ye ◽  
Humaira Rasheed ◽  
Yuehua Ran ◽  
Xiaojuan Yang ◽  
Lianxi Xing ◽  
...  

Abstract Background: The reproductive plasticity of termite workers provides colonies with tremendous flexibility to respond to environmental changes, which is the basis for evolutionary and ecological success. Although it is known that all colony members share the same genetic background and that differences in castes are caused by differences in gene expression, the pattern of the specific expression of genes involved in the differentiation of workers into reproductives remains unclear. In this study, the transition of the female workers into neotenic reproductives (NRs) was induced by a groups of isolated workers (IWs) of Reticulitermes labralis, and then comparative transcriptomes were used for the first time to reveal the molecular mechanisms underlying the reproductive plasticity of workers. Results: We identified 38,070 differentially expressed genes and found profile 5 to be the pattern of gene expression involved in the differentiation of the workers into reproductives. 12,543 genes were specifically upregulated in the IWs. Twenty-five signal transduction pathways classified into environmental information processing were related to the differentiation of workers into NRs. Ras functions as a signalling switch regulated the reproductive plasticity of workers.The catalase gene which is related to longevity was up-regulated in NRs. Conclusion: We demonstrate that workers leaving the natal colony can induce the expression of stage-specific genes in the workers, which leads to the differentiation of workers into queens and suggests that the signal transduction along the Ras-MAPK pathway crucially controls the reproductive plasticity of the workers. This study also provides an important model for revealing the molecular mechanism of longevity changes.


2020 ◽  
Vol 21 (6) ◽  
pp. 2042 ◽  
Author(s):  
Natalia Wojciechowska ◽  
Emilia Wilmowicz ◽  
Katarzyna Marzec-Schmidt ◽  
Agnieszka Ludwików ◽  
Agnieszka Bagniewska-Zadworna

Plant senescence is a highly regulated process that allows nutrients to be mobilized from dying tissues to other organs. Despite that senescence has been extensively studied in leaves, the senescence of ephemeral organs located underground is still poorly understood, especially in the context of phytohormone engagement. The present study focused on filling this knowledge gap by examining the roles of abscisic acid (ABA) and jasmonate in the regulation of senescence of fine, absorptive roots and leaves of Populus trichocarpa. Immunohistochemical (IHC), chromatographic, and molecular methods were utilized to achieve this objective. A transcriptomic analysis identified significant changes in gene expression that were associated with the metabolism and signal transduction of phytohormones, especially ABA and jasmonate. The increased level of these phytohormones during senescence was detected in both organs and was confirmed by IHC. Based on the obtained data, we suggest that phytohormonal regulation of senescence in roots and leaves is organ-specific. We have shown that the regulation of ABA and JA metabolism is tightly regulated during senescence processes in both leaves and roots. The results were discussed with respect to the role of ABA in cold tolerance and the role of JA in resistance to pathogens.


2007 ◽  
Vol 6 (8) ◽  
pp. 1411-1420 ◽  
Author(s):  
Goran Periz ◽  
Darshita Dharia ◽  
Steven H. Miller ◽  
Laura R. Keller

ABSTRACT Lithium (Li+) affects the physiology of cells from a broad range of organisms including plants and both vertebrate and invertebrate animals. Although its effects result presumably from changes in gene expression elicited by its interaction with intracellular signal transduction pathways, the molecular mechanisms of Li+ action are not well understood. The biflagellate green alga Chlamydomonas reinhardtii is an ideal genetic model for the integration of the effects on Li+ on signal transduction, gene expression, and aspects of flagellar biogenesis. Li+ causes C. reinhardtii flagella to elongate to ∼1.4 times their normal length and blocks flagellar motility (S. Nakamura, H. Tabino, and M. K. Kojima, Cell Struct. Funct. 12:369-374, 1987). We report here that Li+ treatment increases the abundance of several flagellar mRNAs, including α- and β-tubulin and pcf3-21. Li+-induced flagellar gene expression occurs in cells pretreated with cycloheximide, suggesting that the abundance change is a response that does not require new protein synthesis. Deletion analysis of the flagellar α1-tubulin gene promoter showed that sequences necessary for Li+-induced expression differed from those for acid shock induction and contain a consensus binding site for CREB/ATF and AP-1 transcription factors. These studies suggest potential promoter elements, candidate factors, and signal transduction pathways that may coordinate the C. reinhardtii cellular response to Li+.


Sign in / Sign up

Export Citation Format

Share Document